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  • richardmitnick 10:56 am on February 16, 2017 Permalink | Reply
    Tags: , Autism, , , Using (MRI) to study the brains of infants who have older siblings with autism   

    From U Washington: “Predicting autism: Researchers find autism biomarkers in infancy” 

    U Washington

    University of Washington

    February 15, 2017
    No writer credit

    By using magnetic resonance imaging (MRI) to study the brains of infants who have older siblings with autism, scientists were able to correctly identify 80 percent of the babies who would be subsequently diagnosed with autism at 2 years of age.

    Researchers from the University of Washington were part of a North American effort led by the University of North Carolina to use MRI to measure the brains of “low-risk” infants, with no family history of autism, and “high-risk” infants who had at least one autistic older sibling. A computer algorithm was then used to predict autism before clinically diagnosable behaviors set in. The study was published Feb. 15 in the journal Nature.

    This is the first study to show that it is possible to use brain biomarkers to identify which infants in a high-risk pool — that is, those having an older sibling with autism — will be diagnosed with autism spectrum disorder, or ASD, at 24 months of age.

    2
    Annette Estes, left, plays with a child at the UW Autism Center.Kathryn Sauber

    “Typically, the earliest we can reliably diagnose autism in a child is age 2, when there are consistent behavioral symptoms, and due to health access disparities the average age of diagnosis in the U.S. is actually age 4,” said co-author and UW professor of speech and hearing sciences Annette Estes, who is also director of the UW Autism Center and a research affiliate at the UW Center on Human Development and Disability, or CHDD. “But in our study, brain imaging biomarkers at 6 and 12 months were able to identify babies who would be later diagnosed with ASD.”

    The predictive power of the team’s findings may inform the development of a diagnostic tool for ASD that could be used in the first year of life, before behavioral symptoms have emerged.

    “We don’t have such a tool yet,” said Estes. “But if we did, parents of high-risk infants wouldn’t need to wait for a diagnosis of ASD at 2, 3 or even 4 years and researchers could start developing interventions to prevent these children from falling behind in social and communication skills.”

    People with ASD — which includes 3 million people in the United States — have characteristic social communication deficits and demonstrate a range of ritualistic, repetitive and stereotyped behaviors. In the United States, it is estimated that up to one out of 68 babies develops autism. But for infants with an autistic older sibling, the risk may be as high as one out of every five births.

    This research project included hundreds of children from across the country and was led by researchers at four clinical sites across the United States: the University of North Carolina-Chapel Hill, UW, Washington University in St. Louis and The Children’s Hospital of Philadelphia. Other key collaborators are at the Montreal Neurological Institute, the University of Alberta and New York University.

    3
    Stephen Dager.Marie-Anne Domsalla

    “We have wonderful, dedicated families involved in this study,” said Stephen Dager, a UW professor of radiology and associate director of the CHDD, who led the study at the UW. “They have been willing to travel long distances to our research site and then stay up until late at night so we can collect brain imaging data on their sleeping children. The families also return for follow-up visits so we can measure how their child’s brain grows over time. We could not have made these discoveries without their wholehearted participation.”

    Researchers obtained MRI scans of children while they were sleeping at 6, 12 and 24 months of age. The study also assessed behavior and intellectual ability at each visit, using criteria developed by Estes and her team. They found that the babies who developed autism experienced a hyper-expansion of brain surface area from 6 to 12 months, as compared to babies who had an older sibling with autism but did not themselves show evidence of autism at 24 months of age. Increased surface area growth rate in the first year of life was linked to increased growth rate of brain volume in the second year of life. Brain overgrowth was tied to the emergence of autistic social deficits in the second year.

    4
    MRI technician Mindy Dixon and Stephen Dager review a magnetic resonance spectroscopic image of a child’s brain chemistry.University of Washington

    The researchers input these data — MRI calculations of brain volume, surface area, and cortical thickness at 6 and 12 months of age, as well as sex of the infants — into a computer program, asking it to classify babies most likely to meet ASD criteria at 24 months of age. The program developed the best algorithm to accomplish this, and the researchers applied the algorithm to a separate set of study participants.

    Researchers found that, among infants with an older ASD sibling, the brain differences at 6 and 12 months of age successfully identified 80 percent of those infants who would be clinically diagnosed with autism at 24 months of age.

    If these findings could form the basis for a “pre-symptomatic” diagnosis of ASD, health care professionals could intervene even earlier.

    “By the time ASD is diagnosed at 2 to 4 years, often children have already fallen behind their peers in terms of social skills, communication and language,” said Estes, who directs behavioral evaluations for the network. “Once you’ve missed those developmental milestones, catching up is a struggle for many and nearly impossible for some.”

    Research could then begin to examine interventions on children during a period before the syndrome is present and when the brain is most malleable. Such interventions may have a greater chance of improving outcomes than treatments started after diagnosis.

    “Our hope is that early intervention — before age 2 — can change the clinical course of those children whose brain development has gone awry and help them acquire skills that they would otherwise struggle to achieve,” said Dager.

    The research team has gathered additional behavioral and brain imaging data on these infants and children — such as changes in blood flow in the brain and the movement of water along white matter networks — to understand how brain connectivity and neural activity may differ between high-risk children who do and don’t develop autism. In a separate study published Jan. 6 in Cerebral Cortex, the researchers identified specific brain regions that may be important for acquiring an early social behavior called joint attention, which is orienting attention toward an object after another person points to it.

    “These longitudinal imaging studies, which follow the same infants as they grow older, are really starting to hone in on critical brain developmental processes that can distinguish children who go on to develop ASD and those who do not,” said Dager. “We hope these ongoing efforts will lead to additional biomarkers, which could provide the basis for early, pre-symptomatic diagnosis and serve also to guide individualized interventions to help these kids from falling behind their peers.”

    The research was funded by the National Institutes of Health, Autism Speaks and the Simons Foundation.

    See the full article here .

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  • richardmitnick 9:41 am on January 16, 2017 Permalink | Reply
    Tags: , Autism, Autism Risk May Arise From Sex-Specific Traits, , , SNP - single nucleotide polymorphism   

    From SA: “Autism Risk May Arise From Sex-Specific Traits” 

    Scientific American

    Scientific American

    January 16, 2017
    Ann Griswold

    Genetic sequences that code for physical features that differ between boys and girls also seem to contribute to risk for the disorder.

    1
    Alena Baranova, EyeEm, Getty Images

    2
    Basic biology: Different genetic variants contribute to autism risk in boys versus girls. Alfred Pasieka / Science Photo Library

    Genetic variants that shape physical features that vary with sex, such as waist-to-hip ratio, may also affect autism risk, according to a new study.

    Many of the genes involved in these features are not linked to autism or even the brain. Instead, they help establish basic physical differences between the sexes, says lead investigator Lauren Weiss, associate professor of psychiatry at the University of California, San Francisco.

    “Whatever general biological sex differences cause a [variant] to have a different effect on things like height in males and females, those same mechanisms seem to be contributing to autism risk,” she says. The work appeared in November in PLOS Genetics.

    The results bolster the notion that mutations in some genes contribute to autism’s skewed sex ratio: The condition is diagnosed in about five boys for every girl. That may be because girls require a bigger genetic hit to show features of the condition, because sex hormones in the womb boost the risk in boys or because autism is easier to detect in boys than in girls.

    The new study is the first to look at sex differences in common genetic variants called single nucleotide polymorphisms (SNPs). It shows that the sexes differ in which autism-linked SNPs they have, but not in the overall number of such SNPs.

    Separate sets:

    Weiss and her team analyzed published genetic data from four databases and unpublished data from five others. Altogether, they reviewed information from 8,646 individuals with autism, including 1,468 girls and women. They also analyzed data from 15,028 controls, some of whom are related to people in the autism group.

    The researchers first identified SNPs that differ between males with autism and their unaffected family members and unrelated controls. They then repeated the procedure for girls and women with autism.

    These two analyses revealed distinct sets of SNPs associated with autism: a set of five SNPs in boys and men and a separate set of three SNPs in girls and women. None of the variants have previously been associated with autism.

    The researchers then compared males who have autism with females who have the condition. They found similar levels of genetic variation in the two groups, with equal numbers of autism risk genes affected. This result suggests that common variants do not contribute to a stronger genetic hit in girls with autism.

    Body of data:

    When the researchers compared people who have autism with controls, they did not find any differences in SNPs in genes that respond to sex hormones.

    The team then looked at 11 SNPs known to influence height, weight, body mass index, hip and waist measurements in women, and 15 variants that influence these physical traits in men. They found more of these sex-specific SNPs in people with autism than in controls. None of these SNPs have previously been associated with autism.

    The findings suggest that different SNPs contribute to autism risk in boys and girls.

    The fact that some of these SNPs also shape physical traits in a sex-specific way is particularly interesting, says Meng-Chuan Lai, assistant professor in psychiatry at the University of Toronto, who was not involved in the study. Scientists should examine whether sex differences in brain structure in people with autism track with the sex-specific SNPs, he says.

    Weiss says she hopes the findings will spur researchers to pay more attention to the influences of sex when sifting through genomic data. Outfitting genetic repositories with the option to sort data by sex would be the next step for that approach.

    See the full article here .

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  • richardmitnick 1:08 pm on December 6, 2016 Permalink | Reply
    Tags: , Autism, ,   

    From UCLA: “Brains of people with autism spectrum disorder share similar molecular abnormalities” 

    UCLA bloc

    UCLA

    December 05, 2016
    Jim Schnabel

    1
    Brains typically have a standard pattern for which genes are active and which are inactive (left). In the brains of people with autism (right), genes don’t follow that pattern, but they do have their own consistent patterns from one brain to the next. Neelroop Parikshak/UCLA Health

    Autism spectrum disorder is caused by a variety of factors, both genetic and environmental. But a new study led by UCLA scientists provides further evidence that the brains of people with the disorder tend to have the same “signature” of abnormalities at the molecular level.

    The scientists analyzed 251 brain tissue samples from nearly 100 deceased people — 48 who had autism and 49 who didn’t. Most of the samples from people with autism showed a distinctive pattern of unusual gene activity.

    The findings, published Dec. 5 in Nature, confirm and extend the results of earlier, smaller studies, and provide a clearer picture of what goes awry, at the molecular level, in the brains of people with autism.

    “This pattern of unusual gene activity suggests some possible targets for future autism drugs,” said Dr. Daniel Geschwind, the paper’s senior author and UCLA’s Gordon and Virginia MacDonald Distinguished Professor of Human Genetics. “In principle, we can use the abnormal patterns we’ve found to screen for drugs that reverse them — and thereby hopefully treat this disorder.”

    According to the Centers for Disease Control and Prevention, about 1.5 percent of children in the U.S. have autism; the disorder is characterized by impaired social interactions and other cognitive and behavioral problems. In rare cases, the disorder has been tied to specific DNA mutations, maternal infections during pregnancy or exposures to certain chemicals in the womb. But in most cases, the causes are unknown.

    In a much-cited study in Nature in 2011, Geschwind and colleagues found that key regions of the brain in people with different kinds of autism had the same broad pattern of abnormal gene activity. More specifically, researchers noticed that the brains of people with autism didn’t have the “normal” pattern for which genes are active or inactive that they found in the brains of people without the disorder. What’s more, the genes in brains with autism weren’t randomly active or inactive in these key regions, but rather had their own consistent patterns from one brain to the next — even when the causes of the autism appear to be very different.

    The discovery suggested that different genetic and environmental triggers of autism disorders mostly lead to disease via the same biological pathways in brain cells.

    In the new study, Geschwind and his team analyzed a larger number of brain tissue samples and found the same broad pattern of abnormal gene activity in areas of the brain that are affected by autism.

    “Traditionally, few genetic studies of psychiatric diseases have been replicated, so being able to confirm those initial findings in a new set of patients is very important,” said Geschwind, who also is a professor of neurology and psychiatry at the David Geffen School of Medicine at UCLA. “It strongly suggests that the pattern we found applies to most people with autism disorders.”

    The team also looked at other aspects of cell biology, including brain cells’ production of molecules called long non-coding RNAs, which can suppress or enhance the activity of many genes at once. Again, the researchers found a distinctive abnormal pattern in the autism disorder samples.

    Further studies may determine which abnormalities are drivers of autism, and which are merely the brain’s responses to the disease process. But the findings offer some intriguing leads about how the brains of people with autism develop during the first 10 years of their lives. One is that, in people with the disorder, genes that control the formation of synapses — the ports through which neurons send signals to each other — are abnormally quiet in key regions of the brain. During the same time frame, genes that promote the activity of microglial cells, the brain’s principal immune cells, are abnormally busy.

    This could mean that the first decade of life could be a critical time for interventions to prevent autism.

    The study also confirmed a previous finding that in the brains of people with autism, the patterns of gene activity in the frontal and temporal lobes are almost the same. In people who don’t have autism, the two regions develop distinctly different patterns during childhood. The new study suggests that SOX5, a gene with a known role in early brain development, contributes to the failure of the two regions to diverge in people with autism.

    The study’s lead authors are Neelroop Parikshak, Vivek Swarup and Grant Belgard of UCLA; other co-authors are Gokul Ramaswami, Michael Gandal, Christopher Hartl, Virpi Leppa, Luis de la Torre Ubieta, Jerry Huang, Jennifer Lowe and Steve Horvath of UCLA; Manuel Irimia of the Barcelona Institute of Science and Technology; and Benjamin Blencowe of the University of Toronto.

    The research was funded in part by the National Institutes of Health.

    See the full article here .

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    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

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  • richardmitnick 5:20 am on September 1, 2016 Permalink | Reply
    Tags: , Autism, , microRNAs,   

    From UCLA: “UCLA study links autism to changes in micro-RNAs” 

    UCLA bloc

    UCLA

    August 31, 2016
    Jim Schnabel

    In an important new study, scientists at UCLA have found that the brains of people with autism spectrum disorders show distinctive changes in the levels of tiny regulator molecules known as microRNAs, which control the activities of large gene networks.

    The study is the first to demonstrate the broad importance of microRNAs in autism disorders. The researchers found evidence that the individual microRNAs implicated in the study regulate many genes previously linked to autism.

    The study thus brings researchers closer to understanding the causes of autism disorders, and in particular why the activities of so many genes are abnormal in these disorders. In principle, microRNAs or related molecules could someday be targeted with drugs to treat or prevent autism.

    “These findings add a new layer to our understanding of the molecular changes that occur in the brains of patients with autism spectrum disorders, and give us a good framework for more detailed investigations of microRNAs’ contributions to these disorders,” said Dr. Daniel Geschwind, principal investigator and the Gordon and Virginia MacDonald Distinguished Professor of Human Genetics in the David Geffen School of Medicine at UCLA.

    The new research, published online in Nature Neuroscience, is by far the most comprehensive autism-related study of microRNAs, small molecules made of single-stranded RNA (ribonucleic acid), DNA’s more primitive cousin. Almost nothing was known about microRNAs before 2001, but researchers have since determined that hundreds of different microRNAs exist in human cells, and collectively regulate the activity of most of our genes.

    Because a typical microRNA reduces the activities of dozens to hundreds of genes, too much or too little of that microRNA can disrupt the normal workings of many cellular processes at once. Unsurprisingly, microRNA abnormalities have already been linked to a variety of disorders, including Alzheimer’s and cancers.

    “Autism is in a sense a good place to look for microRNA abnormalities, because prior studies from our laboratory and others have linked autism disorders to changes in the expression levels of a large number of genes,” said Geschwind, who is also a professor of neurology and psychiatry.

    For the study, Geschwind and colleagues measured levels of nearly 700 microRNAs in samples of brain tissue taken during autopsies of 55 people with autism spectrum disorders, and 42 control subjects without autism disorders. The analysis focused on samples from the cortex, which in most of the autism spectrum disorder cases showed a distinctive “signature” of abnormalities, involving 58 microRNAs — 17 with lower than normal levels and 41 with higher than normal levels.

    Looking at groupings or “modules” of microRNAs that seem to work together in cells, the team found another autism spectrum disorder signature: two distinct modules whose microRNAs were at abnormally high levels in the autism spectrum disorder samples, and one whose microRNAs were at abnormally low levels.

    The affected microRNAs are thought collectively to regulate hundreds of different genes. Among them, the scientists found a disproportionately large number that are already considered “autism risk” genes — typically because mutations or uncommon variants of those genes have been linked to autism spectrum disorders. The genes thought to be regulated by the autism-linked microRNAs also include many whose activity is known to be abnormal in autism, even when there is no obvious autism-risk mutation. Geschwind’s team selected several of the most strongly ASD-linked microRNAs, and confirmed with experiments in cultured brain cells that altering their levels — in the direction seen in the autism spectrum disorder samples — caused the kinds of changes in gene activity that were also seen in these samples.

    “From all this it seems likely that abnormalities in the levels of these microRNAs contribute to the broad gene expression changes we see in the brain in autism,” said Emily Wu, a postdoctoral scholar in the Geschwind Laboratory who was first author of the study and performed most of the experiments.

    The study employed advanced RNA sequencing techniques and was thorough enough to uncover, and link to the autism disorder cases, several microRNAs that had never been described before. One of them, hsa_can_1002-m, turned out to be specific for primates and thus couldn’t have been detected in mouse studies.

    The team plans to follow up by studying these ASD-linked microRNAs in more detail, to better characterize the effects of their altered levels on gene activity, brain development, cognition and behavior. “It would be interesting to test whether manipulating the levels of these microRNAs in animal models of autism can reverse autism-related signs,” Wu said.

    Any clinical payoff from the new research is many years away at best. But success in targeting microRNAs in animal model studies might eventually lead to the development of autism spectrum disorder treatments or even preventive measures. Autism spectrum disorders currently affect about one in 40 boys and one in 200 girls in the United States, and there are no specific therapies.

    The other authors of the study were Neelroop Parikshak, and Grant Belgard, both of UCLA at the time of the study.

    Funding was provided by the US National Institutes of Health (grant R01MH094714).

    See the full article here .

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    UC LA Campus

    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

     
  • richardmitnick 7:58 am on August 13, 2016 Permalink | Reply
    Tags: , Autism, , OCD and Attention Deficit May Share Brain Markers,   

    From SA: “Autism, OCD and Attention Deficit May Share Brain Markers” 

    Scientific American

    Scientific American

    August 9, 2016
    Ann Griswold

    1
    The researchers could distinguish “autism” from “not autism” (control) in 33 of 34 study participants, by using computerized analysis of brain scans showing activity in response to social words such as “hug.” https://www.autismspeaks.org

    Autism shares genetic roots with obsessive-compulsive disorder (OCD) and attention deficit hyperactivity disorder (ADHD). The three conditions have features in common, such as impulsivity. New findings suggest that they also share a brain signature.

    The first comparison of brain architecture across these conditions has found that all are associated with disruptions in the structure of the corpus callosum. The corpus callosum is a bundle of nerve fibers that links the brain’s left and right hemispheres. The results appeared July 1 in the American Journal of Psychiatry.

    Clinicians may find it difficult to distinguish autism from ADHD based on symptoms alone. But if the conditions are marked by similar structural problems in the brain, the same interventions might be useful no matter what the diagnosis is, says lead researcher Stephanie Ameis, assistant professor of psychiatry at the University of Toronto.

    The unique aspects of each condition might arise from other brain attributes, such as differences in the connections between neurons, says Thomas Frazier, director of research at the Cleveland Clinic Foundation. “A reasonable conclusion is that autism and ADHD don’t differ dramatically in a structural way, but could differ in connectivity,” says Frazier, who was not involved in the study.

    Broken links:

    Ameis’ team examined the brains of 71 children with autism, 31 with ADHD, 36 with OCD and 62 typical children using diffusion tensor imaging. This method provides a picture of the brain’s white matter, the long fibers that connect nerve cells, by measuring the diffusion of water across these fibers.

    The researchers saw widespread disruptions in white matter structure among children with any of the three conditions. They found fewer alterations in the children with OCD than in those with autism or ADHD, however.

    This finding may relate to the early onset of autism and ADHD. Localized white matter disruptions may produce problems associated with OCD later in childhood, Ameis says.

    Parents also assessed their children’s attention and social communication skills, obsessive behaviors and ability to perform everyday tasks. Children who showed the least independence on daily tasks have the most significant disruptions in white matter. The researchers found no connection between brain structure and the other behaviors.

    “There is an association between what your brain looks like, in terms of its impairment, and how impaired you are in everyday life,” says Ameis.

    Tracing tracts:

    The researchers also looked for problems in particular white matter tracts. The only tract that looks alike in all three groups is the corpus callosum, suggesting that disruptions of this tract may underlie the features the conditions have in common.

    “What’s interesting is that [the corpus callosum] is one of the first tracts to develop and it’s the largest in the brain. So it could be a tract that creates vulnerability for these neurodevelopmental conditions,” Ameis says.

    The findings are preliminary, however. The researchers detected changes in only a small section of the corpus callosum, so it isn’t clear whether the aberrations they saw are clinically meaningful, says Ruth Carper, assistant research professor of neurosciences at the University of California, San Diego, who was not involved in the study.

    It’s also possible that the differences among the three groups stem from movement in the scanner, a common problem when scanning children with these conditions, Carper says.

    Still, researchers say the findings are an initial step toward teasing out the similarities and differences between the three conditions.

    Never mind statistics: Adults with autism may be happy
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    New study bolsters theory that autism genes work in networks
    Neurons from boys with autism grow unusually fast

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  • richardmitnick 11:24 am on July 27, 2016 Permalink | Reply
    Tags: , Autism, , , T.H. Chan School of Public Health   

    From Harvard: “Study finds induced labor not associated with risk for autism spectrum disorders” 

    Harvard University

    Harvard University

    1
    T.H. Chan School of Public Health

    July 25, 2016
    Marge Dwyer
    617.432.8416
    mhdwyer@hsph.harvard.edu

    2
    No image caption. No image credit.

    Induction of labor appears not to be associated with increased risk of autism spectrum disorders in children in a large new study led by Harvard T.H. Chan School of Public Health. The new finding suggests that concern about autism risk should not factor into clinical decisions about whether or not to induce labor.

    The study will be published online July 25, 2016 in JAMA Pediatrics.

    Autism spectrum disorders (ASD) —a group of permanent developmental disabilities characterized by impairments in social interaction, language development, and repetitive behaviors—are estimated to affect roughly 1 in 90 children in the U.S.

    Labor induction is recommended when labor doesn’t progress on its own and there’s concern that waiting for it to start could endanger the health of the baby or mother. Methods to induce labor include rupturing of membranes, mechanical or pharmacological ripening of the cervix, and administration of oxytocin, either used alone or in combination.

    In 2013, a large study in North Carolina found an association between induction of labor and risk of autism in offspring. The report gained widespread media attention, and although both the paper’s authors and other experts cautioned that the association may not be causal, obstetricians began reporting that some of their patients were expressing concern about or opposition to being induced. The Harvard Chan School researchers decided to further explore whether induction of labor truly causes increased risk of neuropsychiatric disorders, in order to help in weighing the risks and benefits of this common therapeutic intervention.

    “When we used close relatives, such as siblings or cousins, as the comparison group, we found no association between labor induction and autism risk,” said Anna Sara Oberg, research fellow in the Department of Epidemiology at Harvard Chan School and lead author of the study. “Many of the factors that could lead to both induction of labor and autism are completely or partially shared by siblings—such as maternal characteristics or socioeconomic or genetic factors. Finding no association when comparing siblings suggests that previously observed associations could have been due to some of these familial factors—not the result of induction.”

    Working with colleagues from Sweden’s Karolinska Institutet and Karolinska University Hospital, Harvard Medical School, and Indiana University, the Harvard Chan School researchers studied all live births in Sweden from 1992–2005. They followed over 1 million births through 2013, looking for any neuropsychiatric diagnoses and identifying all siblings and maternal first cousins. They also incorporated several measures of the mothers’ health in their analysis.

    Nearly 2% of babies in the study population were diagnosed with autism during the follow-up period, the researchers found. Overall, 11% of the deliveries had involved induction of labor, often occurring in conjunction with pregnancy complications such as gestational diabetes, gestational hypertension, and preeclampsia; 23% of the induced pregnancies were post-term.

    In their initial comparison of individuals who weren’t related to each other, the researchers found an association between labor induction and ASD risk, similar to that previously reported. But when they compared “induction-discordant” siblings (children born to the same mother—in one, labor was induced, in the other, it wasn’t), they no longer saw an association.

    “Overall, these findings should provide reassurance to women who are about to give birth, that having their labor induced will not increase their child’s risk of developing autism spectrum disorders,” said Brian Bateman, anesthesiologist and associate professor of anesthesia at Massachusetts General Hospital and Brigham and Women’s Hospital, Harvard Medical School, and senior author of the study.

    “It is important to note that the findings pertain to the risks associated with labor induction per se, and not the specific method or medication used in the process, including oxytocin,” said Oberg.

    Sonia Hernández-Díaz, professor of epidemiology at Harvard Chan School, was a co-author of the study. Funding for the study came from grants 2012-34 (International Postdoctoral grant) and 340-2013-5867 (Swedish Initiative for Research on Microdata in the Social and Medical Sciences [SIMSAM]) from the Swedish Research Council and grants K08HD075831 and R01HD061817 from the National Institutes of Health Eunice Kennedy Shriver National Institute of Child Health & Human Development.

    “Association of Labor Induction With Offspring Risk of Autism Spectrum Disorders,” Anna Sara Oberg, Brian M. D’Onofrio, Martin E. Rickert, Sonia Hernandez-Diaz, Jeffrey L. Ecker, Catarina Almqvist, Henrik Larsson, Paul Lichtenstein, and Brian T. Bateman, JAMA Pediatrics, online July 25, 2016, doi: 10.1001/jamapediatrics.2016.0965

    See the full article here .

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    Harvard is the oldest institution of higher education in the United States, established in 1636 by vote of the Great and General Court of the Massachusetts Bay Colony. It was named after the College’s first benefactor, the young minister John Harvard of Charlestown, who upon his death in 1638 left his library and half his estate to the institution. A statue of John Harvard stands today in front of University Hall in Harvard Yard, and is perhaps the University’s best known landmark.

    Harvard University has 12 degree-granting Schools in addition to the Radcliffe Institute for Advanced Study. The University has grown from nine students with a single master to an enrollment of more than 20,000 degree candidates including undergraduate, graduate, and professional students. There are more than 360,000 living alumni in the U.S. and over 190 other countries.

     
  • richardmitnick 8:33 am on June 10, 2016 Permalink | Reply
    Tags: , , Autism, Autism may stem—in part—from a disordered sense of touch   

    From AAAS: “Autism may stem—in part—from a disordered sense of touch” 

    AAAS

    AAAS

    Jun. 9, 2016
    Teal Burrell

    1
    A disrupted sense of touch causes autismlike behaviors in mice. ploughmann/iStock.

    Sociability may be skin deep. The social impairments and high anxiety seen in people with autism or related disorders may be partly due to a disruption in the nerves of the skin that sense touch, a new study in mice suggests.

    Autism spectrum disorders are primarily thought of as disorders of the brain, generally characterized by repetitive behaviors and deficits in communication skills and social interaction. But a majority of people with autism spectrum disorders also have an altered tactile sense; they are often hypersensitive to light touch and can be overwhelmed by certain textures. “They tend to be very wary of social touch [like a hug or handshake], or if they go outside and feel a gust of wind, it can be very unnerving,” says neuroscientist Lauren Orefice from Harvard Medical School in Boston.

    An appreciation for this sensory aspect of autism has grown in recent years. The newest version of psychiatry’s bible, the Diagnostic and Statistical Manual of Mental Disorders, includes the sensory abnormalities of autism as core features of the disease. “That was a big nod and a recognition that this is a really important aspect of autism,” says Kevin Pelphrey, a cognitive neuroscientist at The George Washington University in Washington, D.C., who was not involved in the work.

    The sensation of touch starts in the peripheral nervous system—in receptors at the surface of the skin—and travels along nerves that connect into the central nervous system. Whereas many autism researchers focus on the end of the pathway—the brain—Orefice and colleagues wondered about the first leg of the trip. So the group introduced mutations that silenced genes associated with autism spectrum disorders in mice, adding them in a way that restricted the effects to peripheral nerve cells, they report today in Cell. The team singled out the gene Mecp2, which encodes a protein that regulates the expression of genes that help forge connections between nerve cells.

    The Mecp2 mutant mice were more sensitive to light touch; a small puff of air on their backs startled the rodents more than normal mice. Additionally, the mutants were unable to distinguish between rough and smooth textures. Just like normal mice—which love novelty—they played with new objects whenever given a choice between familiar and new ones that differed in shape and size. But when the objects differed by texture, they played just as much with familiar, rough blocks of wood and new, smooth ones—unlike the control mice. Orefice suggests that an increased sensitivity to touch in the mutant mice makes any texture overwhelming, so subtle differences are indistinguishable.

    The animals also displayed autismlike behaviors beyond touch. Even though the defective Mecp2 gene wasn’t present in brain cells, the mutant mice were also more anxious and less social, traits generally attributed to the central nervous system. When given the option to hang out with another mouse or an object like an empty cup, the mutant mice spent just as much time with the object as with the other mouse, unlike normal mice, which prefer a living companion. Tests of anxiety also revealed differences. Whereas normal mice will explore the entirety of an open area or venture onto the wall-less sides of an elevated platform, the mutant mice preferred to hug the edges of the open area and remain in the walled regions of the platform, suggesting heightened anxiety.

    When the researchers silenced the genes in the peripheral nerves of adult animals, they were still hypersensitive to light touch, but they didn’t display the behavioral abnormalities seen in the animals that had the gene silenced from birth. That suggests to Orefice’s team that there is a developmental window of time when touch influences behavior. “The way we navigate our world is largely with a sense of touch,” she says. During development, touch is key to learning how to interact with other animals and the environment. If a light touch from another mouse is uncomfortable, a mouse might learn to avoid its peers in the future. And if the environment itself feels abrasive, the mouse might stop exploring.

    The researchers also found that the peripheral nerves of Mecp2 mutant mice had low levels of a receptor for the neurotransmitter GABA (gamma-aminobutryic acid). Low GABA levels in the brain have previously been linked to autism, but the new finding opens up an unexpected treatment possibility: a drug that restores GABA function in the periphery. “If we can normalize the hypersensitivity to touch, it’s possible that this might help improve anxietylike behaviors and social interaction deficits. This is not to say that the brain is not important,” Orefice says. But targeting the periphery along with the brain may be a way to get at the disease from both ends.

    For now, the findings apply only to mice, which are an imperfect model for complex cognitive disorders such as autism. “For translation to humans, it would be important to know if pharmacological enhancement—ideally of the specific GABA receptor—can alleviate the peripheral hypersensitivity to touch, especially in young children who may be in a critical period of vulnerability,” says Takao Hensch, a neuroscientist at Harvard University who was not involved in the research. He also wonders whether the findings apply to other genetic forms of autism spectrum disorders. Mecp2 has been shown to have unique effects on GABA in the brain; perhaps its peripheral effects are unique as well.

    Still, the finding that dysfunction in the touch system can contribute to behavioral problems is exciting, Pelphrey says. “It gives you a sense of how fundamental these sensory features might be … in terms of mechanistically causing some of the other features,” he says. “It really opens up a different way of thinking about what’s going on.”

    See the full article here .

    The American Association for the Advancement of Science is an international non-profit organization dedicated to advancing science for the benefit of all people.

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  • richardmitnick 12:46 pm on June 9, 2016 Permalink | Reply
    Tags: Another Piece of the Puzzle, , Autism,   

    From UNC: “Another Piece of the Puzzle” 

    U NC bloc

    University of North Carolina

    June 9, 2016
    Mark Derewicz

    1
    UNC researchers continue to discover new pieces of the autism puzzle. Most recently, they’ve collaborated with the Simons Foundation to take part in its SPARK initiative — a genetic study that would recruit thousands of families for autism research. Illustration by Corina Cudebec

    UNC clinical researchers begin the largest-ever genetic study of autism to elucidate the complex genetics of the condition

    If a child has autism, the condition is uniquely their own. The genes involved, how those genes are expressed to give rise to the proteins his or her brain cells need to function, how the neurons are wired to articulate thoughts or navigate social interactions or think through a problem — all of these things are unique to this child.

    “No two children with autism are the same,” UNC-Chapel Hill researcher Gabriel Dichter says, “but the way we try to help kids now is with a one-size-fits-all approach. We use a trial-and-error approach and try to help them with the same interventions to see what works and what doesn’t.” It would be better to know more about what intervention would work best for each child as quickly as possible.

    That’s why UNC — along with 20 other research institutions — is taking on the largest genetic study of autism ever attempted. Researchers will collect DNA and other information from 50,000 people with autism and their immediate family members. UNC was one of three pilot institutions tasked with making sure such an ambitious project was even possible. “It will be the first opportunity the research community has had to understand autism genetics in a way that will allow us, in the future, to match a person’s specific genetic profile with a specific treatment plan,” Dichter says. “That’s the ultimate goal.”

    Dichter, Carolina Institute for Developmental Disabilities (CIDD) Director Joseph Piven, and colleagues across the state are recruiting families with children with autism to be part of this study, called the SPARK initiative (Simons Foundation Powering Autism Research for Knowledge). The UNC team hopes to recruit thousands of families — perhaps even 10,000 — of which they would have access to their full genome sequences.

    To date, approximately 50 genes have been identified that almost certainly play a role in autism, and scientists estimate hundreds more are involved. By studying these genes, their biological consequences, and how they interact with environmental factors, researchers could better understand the condition’s causes, and link possible underlying causes to the spectrum of symptoms, skills, and challenges of people affected.

    Piven’s team at CIDD, home to the federally funded Intellectual and Developmental Disabilities Research Center, is no stranger to this kind of work. For more than 15 years, his group — together with the UNC TEACCH Autism Program — has been building a research registry of families with at least one child with autism (whom have all consented to being contacted by UNC researchers conducting studies).

    These North Carolina families, now more than 6,000 strong, have made it possible for UNC researchers to deepen their understanding of this complex condition and provide numerous intervention strategies, support systems, and diagnostic tools. Piven and Dichter’s team will now tap into that registry to recruit these families, while continually working to add more to the list.

    Mark Zylka is a cell biologist and the incoming director of the UNC Neuroscience Center, which is supporting the SPARK initiative with funds for personnel to boost recruitment efforts. “Those of us in the basic sciences want to partner with clinicians in research projects we hope will ultimately benefit people,” he says. Zylka knows better than most what access to genetic information can mean to a researcher and people with the condition.

    A previous group of scientists discovered through genetic analysis that nearly 1,000 genes are potentially linked to autism in some way. Of those genes, Zylka researched UBE3A, a protein coding gene associated with Angelman Syndrome — a neurodevelopmental disorder characterized by severe intellectual and developmental disability, sleep disturbance, seizures, jerky movements, and a typically happy demeanor. He observed cells from a child with a mutated UBE3A gene and cells from the child’s parents.

    Jason Yi, a postdoctoral fellow in Zylka’s lab, found that a child had a “hyperactive” version of UBE3A. It’s like a broken water faucet — the gene can’t be shut off. In normal brain development, that gene has to be turned on to produce an enzyme that targets proteins to be broken down within cells. It then has to be shut off to avoid too much production of the enzyme. In a child with the UBE3A mutation, the faucet is never turned off. In his parents, the gene works normally.

    “We think it may be possible to tamp down UBE3A in some autism patients to restore normal levels of the enzyme in the brain,” Zylka explains. It’s a long way from the clinic, but his and Yi’s work shows it’s possible to affect the basic biology that plays a role in autism.

    From one generation to the next

    Piven, along with the CIDD, has begun to study the link between autism and Parkinson’s disease. In two small, preliminary clinical studies, he and colleagues found that Parkinson’s disease may occur much more commonly in older adults with autism than in those without autism.

    He and his team identified 20 adults with autism who were not taking atypical neuroleptic drugs. Four of them were diagnosed with Parkinson’s disease. This 20 percent rate of diagnosis was 200 fold higher than the normal rate of incidence — one in 1000 or 0.1 percent — among the general population of people ages 45 to 65. There was an even higher rate of Parkinsonian symptoms among participants with autism who were taking neuroleptic drugs, which can cause the neurological problems seen in Parkinson’s disease.

    The study needs to be replicated in a larger pool of people with autism. “We think these findings are the tip of the iceberg,” Piven says. “Studying older populations of people with autism is a new frontier, and we think this continued work will uncover very important information all of us need in order to better care for people with autism as they age.”

    And that’s a big deal.

    “By and large, what autism is like for older adults is still a mystery,” Piven adds. “Many of these people were misdiagnosed years ago, and there’s nearly nothing in the medical literature about these older people with autism.”

    As UNC basic science researchers delve into the genetics of autism and the potential environmental triggers, UNC behavioral researchers are focused on developing and disseminating community-based services. UNC TEACCH Autism Program director Laura Klinger is busy documenting the needs of adults with autism.

    Research conducted by Julie Daniels at UNC in collaboration with the Centers for Disease Control shows that the prevalence of autism in 8-year-olds has risen from 1 in 150 in 2002 to 1 in 68 in 2012. The first cohort of 8-year-olds is now 22 years of age.

    “So, we can look ahead and expect a large increase in the number of adults with autism in the coming decade,” Klinger said. “Yet, we know very little about how to support a good quality of life for adults with the disorder. We’ve learned so much about autism in children in the past decade. We can diagnose autism earlier than ever before, and we have witnessed firsthand how earlier interventions can make a difference in children’s lives. Now, we need to focus on supporting individuals with autism across the entire lifespan.”

    There is much work to be done in developing vocational, residential, medical, and mental health services to support adults with autism, Klinger adds. “The longevity of autism services and research at UNC gives us a unique opportunity to lead the world in understanding aging in autism.”

    Right now, scientists don’t understand the underlying genetics well enough and don’t have a good enough handle on potential environmental causes, according to Piven. Clinicians are limited in their ability to help some of the more severe cases, though they’ve made strides in the past decade. And the medical community doesn’t have a good concept of what it’s like to live with autism for many decades into old age.

    “The good news is that UNC is one of the few places in the world capable of tackling these and other issues facing the autism community,” Piven says. “We have the scientific and clinical expertise, and we’re making progress every day.”

    Gabriel Dichter is an associate professor of psychiatry and psychology, and also the director of the Clinical Affective Neuroscience Lab at UNC-Chapel Hill.

    Joseph Piven is the Thomas E. Castelloe Distinguished Professor of Psychiatry, Pediatrics, and Psychology; director of the Carolina Institute for Developmental Disabilities; and director of the Intellectual and Developmental Disabilities Research Center, which is funded through the National Institute of Child Health and Development.

    Mark Zylka is the incoming director of the UNC Neuroscience Center. He is also a professor of cell biology and physiology and an adjunct associate professor of pharmacy.

    Laura Klinger is an associate professor in the Department of Psychiatry and Neuroscience and the director of the TEACCH Autism Program.

    See the full article here .

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    U NC campus

    Carolina’s vibrant people and programs attest to the University’s long-standing place among leaders in higher education since it was chartered in 1789 and opened its doors for students in 1795 as the nation’s first public university. Situated in the beautiful college town of Chapel Hill, N.C., UNC has earned a reputation as one of the best universities in the world. Carolina prides itself on a strong, diverse student body, academic opportunities not found anywhere else, and a value unmatched by any public university in the nation.

     
  • richardmitnick 4:13 pm on June 6, 2016 Permalink | Reply
    Tags: , Autism, ,   

    From SA: “Brain Tissue Study Deepens Autism–Schizophrenia Link” 

    Scientific American

    Scientific American

    June 6, 2016
    Sarah DeWeerdt

    1
    Credit: Photo-Dave

    Brains from people with autism show patterns of gene expression similar to those from people with schizophrenia, according to a new analysis.

    The findings, published* May 24 in Translational Psychiatry, deepen the connections between the two conditions, says study leader Dan Arking, associate professor of genetic medicine at Johns Hopkins University in Baltimore, Maryland.

    People who have either autism or schizophrenia share features such as language problems and difficulty understanding other people’s thoughts and feelings. They also have genetic risk factors in common. “And now I think we can show that they share overlap in gene expression,” Arking says.

    The study builds on previous work, in which Arking’s team characterized gene expression in postmortem brain tissue from 32 individuals with autism and 40 controls. In the new analysis, the researchers made use of that dataset as well as one from the Stanley Medical Research Institute that looked at 31 people with schizophrenia, 25 with bipolar disorder and 26 controls3.

    They found 106 genes expressed at lower levels in autism and schizophrenia brains than in controls. These genes are involved in the development of neurons, especially the formation of the long projections that carry nerve signals and the development of the junctions, or synapses, between one cell and the next. The results are consistent with those from previous studies indicating a role for genes involved in brain development in both conditions.

    “On the one hand, it’s exciting because it tells us that there’s a lot of overlap,” says Jeremy Willsey, assistant professor of psychiatry at the University of California, San Francisco, who was not involved in the work. “On the other hand, these are fairly general things that are overlapping.”

    Strong ties:

    Most previous studies of gene expression in autism or schizophrenia did not involve brain tissue: Some relied on blood and others on neurons derived from stem cells. “Having what the brain transcriptome looks like is important,” says Jon McClellan, professor of psychiatry at the University of Washington in Seattle, who was not involved in the work.

    It’s also significant that the common patterns emerged from two disparate datasets involving different study designs and brain regions. “The fact that you have a positive finding, to me, under those circumstances, really says that this is likely to be real,” Arking says.

    In the study, gene expression in schizophrenia and bipolar disorder are not notably similar, even though schizophrenia is thought to have stronger genetic ties to bipolar disorder than to autism. A larger study may reveal an overlap between the two conditions, Arking and others say.

    The similarities in gene expression between schizophrenia and autism could stem from a shared mechanism for the two conditions. Or they may reflect common processes that compensate for the other brain changes, says Shannon Ellis, who conducted the analysis as a graduate student in Arking’s lab. “We can’t say anything about whether this is cause or effect,” she says.

    Flagging genes:

    By comparing the results of genetic studies with gene expression analyses, researchers can glean hints about causal relationships. The genes that show altered expression in people with autism or schizophrenia are not ones that tend to pop up in genome-wide association studies of these disorders. Those studies are designed to reveal common variants that occur more often in people with a condition than in the general population.

    The disparate results from these different kinds of studies suggests that the gene expression changes in autism and schizophrenia brains don’t cause the conditions, Arking says. “What we’re seeing are sort of the downstream consequences of that primary effect,” he says.

    The study does point to new genes that may play a role in the conditions. Two genes located on chromosome 12, called IQSEC3 and COPS7A, are expressed at unusually low levels in autism, schizophrenia and bipolar disorder, the researchers found.

    Relatively little is known about these two genes, and they may not be involved in all cases of these conditions. Still, they are worth following up on, says Arking. IQSEC3, in particular, is dramatically suppressed in all three conditions. “It’s hard to imagine that’s not an important player in some way,” he says.

    *Science paper:
    Transcriptome analysis of cortical tissue reveals shared sets of downregulated genes in autism and schizophrenia

    See the full article here .

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  • richardmitnick 12:01 pm on January 12, 2016 Permalink | Reply
    Tags: , Autism,   

    From UCLA: “Untapped region in brain cell offers goldmine of drug targets for new autism treatments” 

    UCLA bloc

    UCLA

    January 11, 2016

    Elaine Schmidt
    310-794-2272
    eschmidt@mednet.ucla.edu

    1
    Studies have linked mutations in the gene Rbfox1 to a higher risk of autism. Kelsey Martin lab

    CLA scientists have discovered that an overlooked region in brain cells houses a motherlode of mutated genes previously tied to autism. Recently published in Neuron, the finding could provide fresh drug targets and lead to new therapies for the disorder, which affects one in 68 children in the United States.

    “Our discovery will shed new light on how genetic mutations lead to autism,” said principal investigator Dr. Kelsey Martin, interim dean and a professor of biological chemistry at the David Geffen School of Medicine at UCLA. “Before we can develop an effective therapy to target a gene, we must first understand how the gene operates in the cell.”

    The UCLA team focused on a gene called Rbfox1, which regulates how the cell makes proteins — the molecular workhorses that perform essential tasks in cells. Proteins also help shape the body’s tissues and organs, like the brain.

    “Identifying a gene’s function is critical for molecular medicine,” said coauthor Daniel Geschwind, the Gordon and Virginia MacDonald Distinguished Professor of Human Genetics and a professor of neurology and psychiatry at UCLA. “My colleagues discovered that Rbfox1 has an entirely new function that other scientists had overlooked.”

    Earlier studies by Geschwind and others have linked mutations in Rbfox1 to an increased risk for autism, which makes Rbfox1 an especially important gene to study. To better understand how Rbfox1 functions, Martin teamed up with UCLA molecular geneticist Douglas Black. The two blended a cell biology approach with powerful DNA-sequencing technology to reveal the identities of the genes controlled by Rbfox1.

    “Our results turned up an exciting new set of genetic connections,” said Black, a professor of microbiology, immunology and molecular genetics. “We found that where Rbfox1 was located in the cell determined what genes it influenced.”

    First author Ji-Ann Lee, a researcher in Martin’s lab, compared Rbfox1’s function in the cell’s nucleus, or command center, to its function in the cytoplasm, the gel-like fluid that surrounds the cell’s nucleus.

    “Scientists used to think that Rbfox1 worked primarily in the nucleus to allow genes to make multiple proteins. We were surprised to see that Rbfox1 also controls more than 100 genes in the cytoplasm,” Lee said. “A majority of these genes encode proteins critical to the brain’s development and have been tied to autism risk.”

    Furthermore, the genes controlled by Rbfox1 in the cell’s nucleus were completely different from those it controlled in the cell’s cytoplasm.

    The UCLA team’s separation of these two functions revealed that the genes targeted by RBfox1 in the cell’s cytoplasm were highly enriched in proteins vital to the developing brain. Autism risk increases when these genes go awry.

    “While some experts have hinted at the role of cytoplasmic gene control by Rbfox1 in autism risk, no one has systematically explored it in nerve cells before,” said Martin, who is also a professor of psychiatry at UCLA’s Semel Institute for Neuroscience and Human Behavior. “Our study is the first to discover that dozens of autism risk genes have special functions in the cytoplasm and share common pathways in regulating the brain cells.”

    To pinpoint new drug targets, the researchers’ next step will be to learn how Rbfox1 controls genes in the cytoplasm.

    “This is a fundamental discovery that poses significant treatment implications,” Geschwind concluded. “Because so many genes are linked to autism risk, identifying common pathways where these genes overlap will greatly simplify our ability to develop new treatments.”

    The study was supported by the National Institute of Mental Health, National Institute of General Medical Sciences, Howard Hughes Medical Institute and Brain and Behavior Research Foundation. UCLA scientists Andrey Damianov, Chia-Ho Lin, Mariana Fontes, Neelroop Parkshak and Erik Anderson also contributed to the research.

    See the full article here .

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    For nearly 100 years, UCLA has been a pioneer, persevering through impossibility, turning the futile into the attainable.

    We doubt the critics, reject the status quo and see opportunity in dissatisfaction. Our campus, faculty and students are driven by optimism. It is not naïve; it is essential. And it has fueled every accomplishment, allowing us to redefine what’s possible, time after time.

    This can-do perspective has brought us 12 Nobel Prizes, 12 Rhodes Scholarships, more NCAA titles than any university and more Olympic medals than most nations. Our faculty and alumni helped create the Internet and pioneered reverse osmosis. And more than 100 companies have been created based on technology developed at UCLA.

     
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